Exploiting the Fanconi Anemia Pathway for Targeted Anti-Cancer Therapy

摘要: Genome instability, primarily caused by faulty DNA repair mechanisms, drives tumorigenesis. Therapeutic interventions that exploit deregulated in cancer have made considerable progress targeting tumor-specific alterations of factors, which either induces synthetic lethality or augments the efficacy conventional chemotherapy and radiotherapy. The study Fanconi anemia (FA), a rare inherited blood disorder predisposition syndrome, has been instrumental understanding extent to defects contribute FA pathway functions resolve blocked replication forks response interstrand cross-links (ICLs), accumulating knowledge its activation ubiquitin-mediated signaling provided promising therapeutic opportunities for treatment. Here, we discuss recent advances our regulation potential application designing tailored therapeutics take advantage ICL cancer.